While the spread of Salmonella enterica serotype Kentucky resistant to ciprofloxacin across Africa and the Middle-East has been described recently, the presence of this strain in humans, food, various animal species (livestock, pets, and wildlife) and in environment is suspected in other countries of different continents. Here, we report results of an in-depth molecular epidemiological study on a global human and non-human collection of S. Kentucky (n = 70). We performed XbaI-pulsed field gel electrophoresis and multilocus sequence typing, assessed mutations in the quinolone resistance-determining regions, detected β-lactam resistance mechanisms, and screened the presence of the Salmonella genomic island 1 (SGI1). In this study, we highlight the rapid and extensive worldwide dissemination of the ciprofloxacin-resistant S. Kentucky ST198-X1-SGI1 strain since the mid-2000s in an increasingly large number of contaminated sources, including the environment. This strain has accumulated an increasing number of chromosomal and plasmid resistance determinants and has been identified in the Indian subcontinent, Southeast Asia and Europe since 2010. The second substitution at position 87 in GyrA (replacing the amino acid Asp) appeared helpful for epidemiological studies to track the origin of contamination. This global study provides evidence leading to the conclusion that high-level resistance to ciprofloxacin in S. Kentucky is a simple microbiological trait that facilitates the identification of the epidemic clone of interest, ST198-X1-SGI1. Taking this into account is essential in order to detect and monitor it easily and to take rapid measures in livestock to ensure control of this infection.

To determine the epidemiology of outbreaks of avian infl uenza A virus (subtypes H5N1, H9N2) in chickens in Bangladesh, we conducted surveys and examined virus isolates. The outbreak began in backyard chickens. Probable sources of infection included egg trays and vehicles from local live bird markets and larger live bird markets.

The pharmacoeconomic analysis illustrated that allergen-specific immunotherapy with the grass allergen tablet is a cost-effective intervention for the prevention of grass pollen induced rhinoconjunctivitis in Northern European countries, for a tablet price below euro 6. In Germany for example the price of the tablet is euro 2.95 corresponding to a yearly treatment cost of euro 358 - based on a 9-year time horizon.

Risk factors were feeding slaughter remnants of purchased chickens, having a body of water nearby, and contact with pigeons.

The aim of the present study was to investigate the pathology in normal or immunosuppressed chickens followed intravenous or intraperitoneal inoculation with a well-characterized strain of Gallibacterium anatis. Two groups of 30 15-week-old commercial brown laying chickens were used, having been screened and found negative for Gallibacterium organisms. One group was treated with 5-fluorouracil to promote heterophil depletion, while the other was saline treated. Ten days later 15 chickens from each group were inoculated either intravenously or intraperitoneally with 3.3 x 10(7) colony-forming units of G. anatis strain 12656-12. Subsets of chickens were sacrificed at 3, 12 or 24 h post-infection and examined for lesions. Livers and spleens were examined by culture and by fluorescent in situ hybridization. Intravenously infected birds showed severe septicaemic lesions in both the normal and immunosuppressed birds. Mortality was recorded only in the latter, with an overall rate of 73%. The intraperitoneally infected chickens of normal immune status showed various degrees of localized purulent peritonitis at the inoculation site, but in the immunosuppressed birds the entire peritoneum tended to be involved along with the abdominal organs. This was similar to previous descriptions of natural infections and may represent a useful infection model for detailed analysis of Gallibacterium virulence factors and pathogenesis.

No abstract

Two outbreaks of fowl cholera in the avifauna in Denmark, affecting primarily eiders but also cormorants, gulls and oyster-catchers were shown to be caused by the same clone of Pasteurella multocida ssp. multocida by restriction enzyme analysis (REA) and ribotyping, using the enzymes HpaII and HhaI and phenotypic characterization. This observation indicated spread by migratory birds. It was shown that the outbreak clone was closely related to isolates of Pasteurella multocida ssp. multocida obtained from back-yard poultry in Denmark, including chickens, pheasants, turkeys and ducks. The only detectable difference between the outbreak clone and some of these strains concerned the size of one fragment. These results indicate a possible exchange of P. multocida ssp. multocida between populations of wild birds and back-yard poultry.Among the DNA fingerprinting methods used, restriction enzyme analysis offered the highest discrimination among thirty strains obtained from back-yard poultry. The restriction enzymes HpaII and HhaI generated almost the same number of profile types, 17 and 15 respectively, but only HpaII differentiated the outbreak clone from the group of closely related strains isolated from back-yard poultry. Ribotyping, using the same enzymes, resulted in 12 and 10 different profile types, respectively. The outbreak isolates did not harbour any plasmids, while six out of the 30 strains originating from back-yard poultry (20%) carried a cryptic plasmid of approximately 3.4 kb.

Keel bone fractures in laying hens have been described with increasing prevalence from several countries over the last twenty years and are considered one of the greatest welfare problems to the layer industry. In Denmark we have observed fracture prevalence in the range of 53% to 100% in flocks from cage-free systems whereas flock prevalences in birds from enriched cages ranged between 50-98%.Previous research have speculated that the underlying reason for the development of keel bone fractures is trauma in relation to impact of the bird with furniture, other equipment etc. However, little evidence of this theory has been provided. Predisposing factors have also been suggested including genetics of the bird, lack of specific feedstuff components, high egg production, management factors and layer fatigue.This study has addressed the possible pathogenesis of these fractures by pathological characterization of fractures in birds from different production systems. More than 60 keel bones with fractures have been characterized histo-pathologically and by CT scan. This included an assessment of damage to muscles and soft tissues, the bone and the healing process including callus formation. This investigation has shown that high energy collisions cannot be responsible for the majority of fractures, located at the caudal tip of the keel bone, observed in laying birds as markers associated trauma were not observed in the majority of the cases just as few recognized healing processes were observed. These results suggest an alternative pathogenesis to trauma. OPEN ACCESS Citation: Thøfner I, Hougen HP, Villa C, Lynnerup N, Christensen JP (2020) Pathological characterization of keel bone fractures in laying hens does not support external trauma as the underlying cause. PLoS ONE 15(3): e0229735.